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01 January 2022, Volume 17 Issue on line Previous Issue    Next Issue

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In vivo neuronal and astrocytic activation of somatosensory cortex by acupuncture stimuli Xiao-Yue Chang, Kai Chen, Tong Cheng, Pui To Lai, Li Zhang, Kwok-Fai So, Edward S. Yang 2022, 17 (on line):  1-5.  Abstract ( 144 )   PDF (2535KB) ( 128 )   Save Current knowledge for the neural mechanism of acupuncture is far from complete. Using two-photon in vivo calcium recording, we found that the acupuncture stimuli in peripheral acupoints potentiated calcium signals of pyramidal neurons in the somatosensory cortex and resulted in late-onset calcium transients in astrocytes. Chemogenetic inhibition of neurons augmented those astrocytic activities. Our results provide evidence for the involvement of both neurons and astrocytes in acupuncture treatment. This study was approved by the Ethics Committee of Experimental Animals of Jinan University. Related Articles | Metrics

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Recent developments of neuroprotective agents for degenerative retinal disorders Kepeng Ou, Youjian Li, Ling Liu, Hua Li, Katherine Cox, Jiahui Wu, Jian Liu, Andrew D. Dick 2022, 17 (on line):  1-12.  Abstract ( 198 )   PDF (1733KB) ( 189 )   Save Retinal degeneration is a debilitating ocular complication characterized by the progressive loss of photoreceptors and other retinal neurons, which are caused by a group of retinal diseases affecting various age groups, and increasingly prevalent in the elderly. Age-related macular degeneration, diabetic retinopathy and glaucoma are among the most common complex degenerative retinal disorders, posing significant public health problems worldwide largely due to the ageing society and the lack of effective therapeutics. Whilst pathoetiologies vary, if left untreated, loss of retinal neurons can result in an acquired degeneration and ultimately severe visual impairment. Irrespective of underlined etiology, loss of neurons and supporting cells including retinal pigment epithelium, microvascular endothelium, and glia, converges as the common endpoint of retinal degeneration and therefore discovery or repurposing of therapies to protect retinal neurons directly or indirectly are under intensive investigation. This review overviews recent developments of potential neuroprotectants including neuropeptides, exosomes, mitochondrial-derived peptides, complement inhibitors, senolytics, autophagy enhancers and antioxidants either still experimentally or in clinical trials. Effective treatments that possess direct or indirect neuroprotective properties would significantly lift the burden of visual handicap. Related Articles | Metrics

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Construction and imaging of a neurovascular unit model Taiwei Dong, Min Li, Feng Gao, Peifeng Wei, Jian Wang 2022, 17 (on line):  1-10.  Abstract ( 95 )   PDF (1332KB) ( 471 )   Save In 2001, the concept of the neurovascular unit (NVU) was introduced at the Stroke Progress Review Group meeting. The NVU is an important element of the health and disease status of blood vessels and nerves in the central nervous system. Since then, the NVU has attracted increasing interest from research teams, who have contributed greatly to the prevention, treatment, and prognosis of stroke and neurodegenerative diseases. However, additional research is needed to establish an efficient, low-cost, and low-energy in vitro model of the neurovascular unit, as well as enable noninvasive observation of neurovascular units in vivo and in vitro. In this review, we first summarize the composition of neurovascular units, then investigate the efficacy of different types of stem cells and cell culture methods in the construction of neurovascular unit models, and finally assess the progress of imaging methods used to observe neurovascular units in recent years and their positive role in the monitoring and investigation of the mechanisms of a variety of central nervous system diseases. Related Articles | Metrics

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Expression and regulatory network of long noncoding RNA in rats after spinal cord hemisection injury Wei Liu, Jin-Cheng Tao, Sheng-Ze Zhu, Chao-Lun Dai, Ya-Xian Wang, Bin Yu, Chun Yao, Yu-Yu Sun 2022, 17 (on line):  1-5.  Abstract ( 129 )   PDF (1699KB) ( 94 )   Save Long noncoding RNAs (lncRNAs) participate in a variety of biological processes and diseases. However, the expression and function of lncRNAs after spinal cord injury has not been extensively analyzed. In this study of right side hemisection of the spinal cord at T10, we detected the expression of lncRNAs in the proximal tissue of T10 lamina at different time points and found 445 lncRNAs and 6522 mRNA were differentially expressed. We divided the differentially expressed lncRNAs into 26 expression trends and analyzed Profile 25 and Profile 2, the two expression trends with the most significant difference. Our results showed that the expression of 68 lncRNAs in Profile 25 rose first and remained high 3 days post-injury. There were 387 mRNAs co-expressed with the 68 lncRNAs in Profile 25. The co-expression network showed that the co-expressed genes were mainly enriched in cell division, inflammatory response, FcγR-mediated cell phagocytosis signaling pathway, cell cycle and apoptosis. The expression of 56 lncRNAs in Profile2 first declined and remained low after 3 days post-injury. There were 387 mRNAs co-expressed with the 56 lncRNAs in Profile 2. The co-expression network showed that the co-expressed genes were mainly enriched in the chemical synaptic transmission process and in the signaling pathway of neuroactive ligand-receptor interaction. The results provided the expression and regulatory network of the main lncRNAs after spinal cord injury and clarified their co-expressed gene enriched biological processes and signaling pathways. These findings provide a new direction for the clinical treatment of spinal cord injury. This study was approved by the Jiangsu Province Animal Ethics Committee of China (approval No. 20180304-008). Related Articles | Metrics

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microRNA-455-5p alleviates neuroinflammation in cerebral ischemia/reperfusion injury Jian-Song Zhang, Pin-Pin Hou, Shuai Shao, Anatol Manaenko, Zhi-Peng Xiao, Yan Chen, Bing Zhao, Feng Jia, Xiao-Hua Zhang, Qi-Yong Mei, Qin Hu 2022, 17 (on line):  1769-1775.  Abstract ( 119 )   PDF (2493KB) ( 91 )   Save Neuroinflammation is a major pathophysiological factor that results in the development of brain injury after cerebral ischemia/reperfusion. Downregulation of microRNA (miR)-455-5p after ischemic stroke has been considered a potential biomarker and therapeutic target for neuronal injury after ischemia. However, the role of miR-455-5p in the post-ischemia/reperfusion inflammatory response and the underlying mechanism have not been evaluated. In this study, mouse models of cerebral ischemia/reperfusion injury were established by transient occlusion of the middle cerebral artery for 1 hour followed by reperfusion. Agomir-455-5p, antagomir-455-5p, and their negative controls were injected intracerebroventricularly 2 hours before or 0 and 1 hour after middle cerebral artery occlusion (MCAO). The results showed that cerebral ischemia/reperfusion decreased miR-455-5p expression in the brain tissue and the peripheral blood. Agomir-455-5p pretreatment increased miR-455-5p expression in the brain tissue, reduced the cerebral infarct volume, and improved neurological function. Furthermore, primary cultured microglia were exposed to oxygen-glucose deprivation for 3 hours followed by 21 hours of reoxygenation to mimic cerebral ischemia/reperfusion. miR-455-5p reduced C-C chemokine receptor type 5 mRNA and protein levels, inhibited microglia activation, and reduced the production of the inflammatory factors tumor necrosis factor-α and interleukin-1β. These results suggest that miR-455-5p is a potential biomarker and therapeutic target for the treatment of cerebral ischemia/reperfusion injury and that it alleviates cerebral ischemia/reperfusion injury by inhibiting C-C chemokine receptor type 5 expression and reducing the neuroinflammatory response.  Related Articles | Metrics